Research
Featured Research Areas
Our lab is focused on developing targeted strategies to improve cardiac repair and reduce adverse remodeling following myocardial infarction.
T Cell Lymphopenia in IHF
Lymphopenia, or reduced lymphocyte count, is commonly observed in many diseases and is increasingly recognized in patients following myocardial infarction (MI). Clinical studies show that lower lymphocyte levels are associated with worse cardiac outcomes, including impaired heart function, increased microvascular obstruction, and poorer prognosis after MI. Given that lymphocytes play protective roles in post-MI cardiac repair and remodeling, severe lymphopenia may weaken adaptive immune responses and impair myocardial healing.
Thymic Involution, Aging and MI
The thymus is essential for T cell development and immune competence, but undergoes progressive age-associated involution that reduces naïve T cell output over time. Although traditionally considered minimally functional in adulthood, emerging evidence indicates the adult thymus remains important for maintaining immune homeostasis. The thymus is highly sensitive to systemic stressors and injury, including myocardial infarction (MI), which activates the hypothalamic-pituitary-adrenal axis and increases glucocorticoid levels. Following MI, elevated glucocorticoids induce thymocyte apoptosis, impair thymic T cell development, and reduce peripheral T cell production, linking cardiac injury to systemic immune suppression.
Innate Immune Memory
Myocardial infarction (MI) triggers a robust inflammatory response characterized by rapid infiltration of innate immune cells to the site of injury. While this response is essential for tissue repair, excessive or dysregulated inflammation can drive adverse cardiac remodeling and worsen patient outcomes. Previously, innate immunity was classified by its inability to generate immunological memory, but studies have shown that various stimuli can result in the two arms of innate immune memory: trained immunity and immune tolerance. Trained immunity is distinct due to a heightened inflammatory response to a subsequent challenge compared with the initial stimulus, whereas immune tolerance is characterized by a diminished inflammatory response upon secondary stimulation.
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